Type I diabetes, juvenile diabetes or insulin-dependent diabetes mellitus is a disease that affects children and young adults. The clinical features of the disease are caused by an insufficiency in the body's own insulin production due to the (near) total destruction of the insulin production. It has been found that this type of diabetes is an autoimmune disease (cf. Castano, L. and G. S. Eisenbirth (1990) Type I diabetes: A chronic autoimmune disease of human, mouse and rat. Annu. Rev. Immunol. 8:647-679).
In the autoimmune destruction of the .beta. cells all cells of the immune system play a more or less important role. The B lymphocytes produce autoantibodies, whereas the monocytes/macrophages are probably involved in the induction of autoimmunity as antigen presenting cells.
It is assumed that T lymphocytes play a major role as effector cells in the destruction reaction. Like most autoimmune diseases type I diabetes arises because the tolerance of the T cells towards the body's own tissue ("self") is lost. The loss of tolerance towards .beta. cells will thus result in the destruction thereof and diabetes will arise.
Furthermore, T cells carry the autoimmune memory. This will inter alia present a problem in transplantation of .beta. cells. As a result of the renewed contact between the T memory cells and the new cells he memory cells will be reactivated leading to a secondary destruction of the cells. This will eventually result in the recurrence of the original autoimmune disease.